INTERNAL MEDICINE BOARDS - PART 7 pot

Seen in patients with prolonged neutropenia, advanced AIDS, diabetes, and chronic granulomatous disease as well as in those on high-dose steroids or immunosuppressants.. neoformans is th

immune status, and geographic location In the United States, infection(33%), cancer (25%), and, to a lesser extent, autoimmune diseases (13%) areresponsible for most identified cases Infection is likely if the patient is older

or from a developing country, as well as in the setting of nosocomial, tropenic, or HIV-associated FUO Etiologies are as follows:

neu-■ Infectious: TB, endocarditis, and occult abscesses are the most common

infectious causes of FUO in immunocompetent patients Consider 1°HIV infection or opportunistic infections due to unrecognized HIV

■ Neoplastic: Lymphoma and leukemia are the most common cancers

causing FUO Other causes include hepatoma, renal cell carcinoma, andatrial myxoma

■ Autoimmune: Adult Still’s disease, SLE, cryoglobulinemia, polyarteritis

nodosa, giant cell (temporal) arteritis/polymyalgia rheumatica (more mon in the elderly)

com-■ Miscellaneous: Other causes of FUO include drug fever, hyperthyroidism

or thyroiditis, Crohn’s disease, Whipple’s disease, familial Mediterraneanfever, recurrent pulmonary embolism, retroperitoneal hematoma, and fac-titious fever

■ In roughly 10–15% of cases, the cause is not diagnosed Most of these cases resolve spontaneously.

E XAM

Repeated physical exams may yield subtle findings in the fundi, conjunctivae,

sinuses, temporal arteries, and lymph nodes Heart murmurs, splenomegaly, andperirectal or prostatic fluctuance/tenderness should be assessed

D IAGNOSIS

■ History: Ask about immune status, cardiac valve disorders, drug use, travel,

TB exposure history, exposure to animals and insects, occupational history,all medications (prescription, over-the-counter, and herbals), sick contacts,and family history of fever

■ Labs/imaging:

■ Obtain routine labs, blood cultures (off antibiotics; hold culture bottlesfor two weeks), CXR, and PPD If indicated, obtain cultures of otherbody fluids (sputum, urine, stool, CSF) as well as a blood smear(malaria, babesiosis) and an HIV test

■ Echocardiography for vegetations; CT/MRI if neoplasms or abscessesare suspected

■ Use more specific tests selectively (ANA, RF, viral cultures, gen tests for viral and fungal infections)

antibody/anti-■ Invasive procedures are generally low yield except for temporal arterybiopsy in the elderly, liver biopsy in patients with LFT abnormalities, andbone marrow biopsy for HIV

T REATMENT

■ If there are no other symptoms, treatment may be deferred until a tive diagnosis is made

defini-■ Broad-spectrum antibiotics if the patient is severely ill or neutropenic

FUO is most commonly due to

unusual presentations of

common diseases rather than

to rare diseases.

Table 11.4 outlines the causes and treatment of food-borne illness, grouped

according to incubation period

F U N G A L I N F E C T I O N S

See Figure 11.2 for typical forms of fungi that might be seen in tissues

exam-ined by histopathology Common fungal infections are discussed below

Candidiasis

The opportunistic yeast Candida is a commensal found on the skin, GI tract,

and female genital tract Superficial infection is especially common among

diabetics Risk factors for deep or disseminated infection include immune

compromise (HIV, malignancy, neutropenia, or steroids), multiple or

pro-longed antibiotic treatment, and invasive procedures C albicans is the most

common cause

S YMPTOMS /E XAM /D IAGNOSIS

■ Candiduria: Yeast in urine usually represents colonization and not

infec-tion Seen in patients with Foley catheters or antibiotic use Diagnose

in-fection by detecting pyuria or yeast in urine casts; treat if the patient is

symptomatic or neutropenic, has undergone renal transplant, or is

await-ing urinary tract procedures

■ Intertrigo (“diaper rash”): Pruritic vesiculopustules rupture to form

mac-erated or fissured beefy-red areas at skin folds Satellite lesions may be

pre-sent Seen in both immunocompetent and immunosuppressed patients

■ Oral thrush: Presents with burning sensations of the tongue or mucosa

with white, curdlike patches that can be scraped away to reveal a raw

surface Seen in patients with AIDS or malignancy or in those who use

in-haled steroids for asthma Diagnosis can be confirmed with KOH prep or

Gram stain

■ Candidal esophagitis: Presents with dysphagia, odynophagia, and

subster-nal chest pain Seen in patients with AIDS, leukemia, and lymphoma

Di-agnosed by the endoscopic appearance of white patches or from biopsy

showing mucosal invasion May occur concurrently with HSV or CMV

esophagitis

■ Candidemia and disseminated candidiasis: Diagnose through cultures of

blood, body fluids, or aspirates Mortality is 40% Candidemia may lead to

endophthalmitis (eye pain, blurred vision), osteomyelitis, arthritis, or

en-docarditis

■ Hepatosplenic candidiasis: Presents with fever and abdominal pain that

emerge as neutropenia resolves following bone marrow transplant

Associ-ated with a high mortality rate Diagnosed by ultrasound or CT imaging

showing abscesses Blood cultures are frequently 

T REATMENT

■ Candiduria: Most cases do not need treatment.

■ Intertrigo and oral thrush: May be treated with topical antifungals

(ny-statin, clotrimazole or miconazole creams, or nystatin suspension swish

T A B L E 1 1 4 Causes of Food-Borne Illness

Ciguatera (grouper, Neurotoxin from algae Perioral paresthesias and shooting pains in Emetics/lavage

snapper) that grow in tropical the legs (may persist for months); within three hours;

reefs bradycardia/hypotension if severe IV fluids;

atropine/pressors, mannitol.

Scombroid (tuna, mahi- Histamine-like substance Burning mouth/metallic taste; flushing, Antihistamines.

mahi, mackerel) in spoiled fish dizziness, headache, GI symptoms;

urticaria/bronchospasm if severe.

MSG poisoning (“Chinese Acetylcholine Burning sensation in the neck/chest/ No treatment.

restaurant syndrome”) abdomen/extremities; sweating,

bronchospasm, tachycardia.

Incubation period 2–14 hours: likely toxin

S aureus(dairy, eggs, Preformed heat-stable Vomiting, epigastric pain No treatment.

mayonnaise, meat products) enterotoxin.

Bacillus cereus Preformed toxin (like Vomiting, epigastric pain, diarrhea No treatment.

S aureus) or sporulation and toxin production in

vivo (like C perfringens).

Clostridium perfringens Toxin is released after Lower GI symptoms No treatment.

(frequently from reheated heat-resistant clostridial

meats, stews, gravies) spores germinate in

the intestines.

Campylobacter(most Fever, diarrhea Ciprofloxacin or

Salmonella Same as above Same as above.

Shigella Shiga toxin Same as above Same as above.

ciprofloxacin.

Vibrio parahaemolyticus Same as above No treatment.

(undercooked seafood)

■ Esophagitis and other deep or disseminated infections: Systemic therapy

with fluconazole, amphotericin, voriconazole, or caspofungin

■ Replace vascular catheters at a new site (do not exchange over a wire!)

■ C albicans is usually susceptible to fluconazole and can be distinguished

from other etiologic agents within several hours by a  germ tube test

(i.e., the yeast grows a germ tube or pseudohyphae) Patients who have

been on fluconazole prophylaxis may have resistant C albicans or

non-albicans species (e.g., C glabrata, C krusei).

C OMPLICATIONS

Patients with persistent candidemia after catheter removal may have

periph-eral septic thrombophlebitis or septic thrombosis of the central veins

Aspergillosis

Aspergillus fumigatus and other species are widespread in soil, water, compost,

potted plants, ventilation ducts, and marijuana

S YMPTOMS /E XAM

■ Allergic bronchopulmonary aspergillosis (ABPA): Presents with episodic

bronchospasm, fever, and brown-flecked sputum Seen in patients with

underlying asthma or CF CXR shows patchy, fleeting infiltrates and lobar

consolidation or atelectasis Labs show eosinophilia, elevated serum IgE,

andserum IgG precipitins

■ Aspergilloma of the lungs or sinus: May be asymptomatic or present with

hemoptysis, chronic cough, weight loss, and fatigue Seen in patients with

previous TB, sarcoidosis, emphysema, or PCP CXR and CT may show an

air-crescent sign or a rim of air around a fungus ball in a preexisting upper

lobe cavity Labs show serum IgG precipitins

■ Invasive aspergillosis:

■ Presents with dry cough, pleuritic chest pain, and persistent fever with

a new infiltrate or nodule despite broad-spectrum antibiotics Seen in

patients with prolonged neutropenia, advanced AIDS, diabetes, and

chronic granulomatous disease as well as in those on high-dose steroids

or immunosuppressants

T A B L E 1 1 4 Causes of Food-Borne Illness (continued)

Enterohemorrhagic E coli Shiga toxin Usually afebrile; bloody diarrhea; HUS in No antibiotics (may

ground beef, contaminated

produce)

Enterotoxigenic E coli Enterotoxins Usually afebrile; diarrhea Ciprofloxacin.

(“traveler’s diarrhea”)

Norwalk-like virus (cruise Usually afebrile; vomiting, headaches, No treatment.

in-■ Labs: The Aspergillus galactomannan assay is approved for diagnosis in

patients with hematologic malignancies and following bone marrowtransplant IgG precipitins and blood cultures are rarely  In high-riskpatients, sputum or bronchial washing cultures are strongly sugges-tive, but definitive diagnosis requires a biopsy demonstrating tissue in-vasion

■ Patients are often severely ill, and empiric antifungal therapy may be reasonable in high-risk patients.

D IFFERENTIAL

■ ABPA: TB, CF, lung cancer, eosinophilic pneumonia, bronchiectasis.

■ Aspergilloma: Invasive aspergillosis.

F I G U R E 1 1 2 Characteristic forms of fungi in human tissue (37 °C).

(Reproduced, with permission, from Bhushan V, Le T First Aid for the USMLE Step 1: 2005.

New York: McGraw-Hill, 2005: 191.)

Endemic mycoses:

Coccidioides immitis

■ ABPA: Systemic corticosteroids plus itraconazole × 8 months improves

lung function and ↓ steroid requirements

■ Aspergilloma: Surgical excision for massive hemoptysis Antifungals play a

limited role

■ Invasive aspergillosis: Voriconazole, amphotericin, or caspofungin.

C OMPLICATIONS

■ ABPA: Bronchiectasis, pulmonary fibrosis.

■ Aspergilloma: Massive hemoptysis; contiguous spread to the pleura or

ver-tebrae

■ Invasive aspergillosis: High mortality, especially in bone marrow and liver

transplant patients

Cryptococcosis

Cryptococcus neoformans is an encapsulated budding yeast found worldwide

in soil, bird (pigeon) droppings, and eucalyptus trees Risk factors for the

dis-ease are HIV-related immunosuppression, Hodgkin’s disdis-ease, leukemia, and

steroid use C neoformans is the most common fungal infection in AIDS

pa-tients (usually associated with a CD4 count < 100) and is the most common

cause of fungal meningitis in all patients

S YMPTOMS /E XAM

■ Meningitis: Mental status changes, headache, nausea, cranial nerve

palsies HIV patients usually lack obvious meningeal signs.

■ May also cause atypical pneumonia (pulmonary infection is usually

asymptomatic) or skin lesions (umbilicated papules resembling

mollus-cum contagiosum), or may involve the bone, eye, or GU tract

D IFFERENTIAL

Meningitis due to TB, neurosyphilis, toxoplasmosis, coccidioidomycosis,

histoplasmosis, HSV encephalitis, meningeal metastases

D IAGNOSIS

■ LP: Patients often have high opening pressure, low glucose, high protein,

and lymphocytic pleocytosis Patients with more advanced

immunosup-pression may have a bland CSF profile even with meningitis India ink

or Gram stain of CSF may show budding yeast with a thick capsule (both

are< 50% sensitive)

■ Polysaccharide cryptococcal antigen (CrAg) in serum or CSF: Serum

CrAg is > 99% sensitive in AIDS patients with meningitis but is less

sensi-tive in non-AIDS patients CSF CrAg is only 90% sensisensi-tive A serum CrAg

titer of > 1:8 indicates active disease

■ Fungal culture of blood, CSF, urine, sputum, or bronchoalveolar lavage.

■ CT or MRI may show hydrocephalus or occasionally nodules

(cryptococ-comas)

Cryptococcemia (a serum CrAg or blood culture) indicates disseminated disease even with a normal LP.

Unlike what is typically seen in bacterial meningitis, HIV patients with cryptococcal meningitis often have minimal symptoms and a bland CSF.

■ HIV- patients: For mild to moderate lung disease, treat with oral

flucona-zole × 6–12 months For meningitis, cryptococcemia, or severe lung ease, treat with amphotericin plus 5-flucytosine × 2 weeks followed by oralfluconazole 400 mg/day for at least 10 weeks

■ For meningitis, give induction/consolidation therapy with

ampho-tericin plus 5-flucytosine × 2 weeks followed by oral fluconazole 400mg/day× 10 weeks

■ Patients with HIV need long-term maintenance therapy with oral

flu-conazole 200 mg/day It may be reasonable to stop prophylaxis if the CD4count↑ to > 100–200 for > 6 months in response to antiretrovirals

■ Repeat LP until symptoms resolve in patients with coma or other signs of

Coccidioidomycosis

Coccidioides immitis is found in the arid southwestern United States, central

California, northern Mexico, and Central and South America It is found insoil, and outbreaks occur after earthquakes or dust storms Risk factors includeexposure to soil and the outdoors (construction workers, archaeologists, farm-ers)

S YMPTOMS /E XAM

■ 1 ° infection (“valley fever,” “desert rheumatism”): Usually presents with

self-limited flulike symptoms, fever, dry cough, pleuritic chest pain, and

headache, often accompanied by arthralgias, erythema nodosum, or thema multiforme CXR may be normal or may show unilateral infil-

ery-trates, nodules, or thin-walled cavities Some patients (5%) may developchronic pneumonia, ARDS, or persistent lung nodules

■ Disseminated disease (1%): Chronic meningitis, skin lesions (papules,

pustules, warty plaques), osteomyelitis, or arthritis

■ Histology may show giant spherules in infected tissues.

Serum CrAg titers are not

useful for monitoring

treatment response of

meningitis in immunosuppressed patients.

CSF CrAg titers should ↓

during successful treatment.

■ Cultures of respiratory secretions or aspirates of bone and skin lesions may

grow the organism (alert the laboratory if the diagnosis is suspected;

Coc-cidioides is highly infectious to lab workers).

T REATMENT

■ Treatment may not be necessary for acute disease but may be reasonable

in patients at risk for dissemination

■ Fluconazole, itraconazole, or amphotericin for disseminated disease

C OMPLICATIONS

Disseminated disease is more common in nonwhites, pregnant women, and

patients with HIV, diabetes, or immunosuppression

Histoplasmosis

Histoplasma capsulatum is found in the Mississippi and Ohio River valleys.

The organism is found in moist soil and in bat and bird droppings Risk

fac-tors include exploring caves and cleaning chicken coops or attics

S YMPTOMS /E XAM

■ 1 ° infection: Most patients are asymptomatic However, patients may

present with fever, dry cough, and substernal chest discomfort CXR may

show patchy infiltrates that become nodular or exhibit multiple small

nod-ules and hilar or mediastinal adenopathy Some patients may develop

chronic upper lobe cavitary pneumonia or mediastinal fibrosis (dysphagia,

SVC syndrome, or airway obstruction)

■ Disseminated disease: Presents with hepatosplenomegaly, adenopathy,

painless palatal ulcers, meningitis, and pancytopenia from bone marrow

infiltration Patients with HIV may develop colonic disease (diarrhea,

per-foration or obstruction from mass lesions)

■ Histology with silver stain of bone marrow, lymph node, or liver.

■ Cultures of blood or bone marrow are  in immunosuppressed patients

with disseminated disease

■ Serologic tests (complement fixation and immunodiffusion assays) are

of-tenin immunocompetent patients

T REATMENT

■ Treatment is not needed for acute pulmonary disease

■ Itraconazole or amphotericin for chronic cavitary pneumonia, mediastinal

fibrosis, or disseminated histoplasmosis

C OMPLICATIONS

Severe or disseminated disease is more common in patients infected with a

large inoculum and in elderly, immunosuppressed, and HIV patients

Blastomyces dermatitidis is found in the central United States (as is

Histo-plasma) as well as in the upper Midwest and Great Lakes regions Risk factors

include exposure to woods and streams

S YMPTOMS /E XAM

Acute pneumonia May lead to warty, crusted, or ulcerated skin lesions or to

osteomyelitis, epididymitis, or prostatitis

D IAGNOSIS

Microscopy and culture of respiratory secretions; biopsy or aspirate material

shows large yeast with broad-based budding.

GI infection, especially Campylobacter enteritis, CMV, EBV, or mycoplasmal

infection Differential diagnosis includes the following:

■ Focal cord lesion: Usually asymmetric; shows early sphincter

involve-ment

■ Rabies: Follows wild animal exposure.

■ West Nile virus.

■ Botulism: Also presents with diplopia and ocular palsies.

■ Tick paralysis: Look for an attached tick, frequently on the scalp.

■ Polio: Usually asymmetric; fever is present.

■ Toxins: Heavy metals, organophosphates.

H A N TAV I R U S P U L M O N A RY SY N D R O M E

First identified in the southwestern United States in 1993; cases have since

been reported across the country Infection follows inhalation of aerosols of dried rodent urine, saliva, or feces The disease begins as a nonspecific febrile syndrome (sudden fever, myalgias) with rapid progression to respira-

tory failure/ARDS and shock Patients have leukocytosis, hemoconcentration,and thrombocytopenia Diagnose by serology or by immunohistochemical

staining of sputum or lung tissue Ribavirin has been used experimentally,

but mortality remains 50%

H U M A N I M M U N O D E F I C I E N C Y V I R U S ( H I V )

HIV targets and destroys CD4+ T lymphocytes, leading to AIDS Risk factorsinclude unprotected sexual intercourse, IV drug use, maternal infection,needlesticks, and mucosal exposure to body fluids; also at risk are patientswho received blood products before 1985 Prognostic factors are CD4 countand HIV RNA viral load CD4 count measures the degree of immune com-promise and predicts the risk of opportunistic infections; viral load measuresHIV replication rate, gauges the efficacy of antiretrovirals, and predicts CD4count decline

■ 1 ° HIV infection: May be asymptomatic Acute retroviral syndrome

pre-sents 2–6 weeks after initial infection with fever, sore throat,

lym-phadenopathy, and a truncal maculopapular rash or mucocutaneous

ul-cerations Other signs and symptoms include myalgias, arthralgias,

diarrhea, headache, nausea, vomiting, weight loss, aseptic meningitis, and

thrush

■ Chronic HIV infection: Fatigue, fevers, night sweats, diarrhea, persistent

lymphadenopathy, and weight loss Suspect in patients with thrush, oral

hairy leukoplakia, herpes zoster, seborrheic dermatitis, oral aphthous

ul-cers, or recurrent vaginal candidiasis

D IFFERENTIAL

Acute retroviral syndrome resembles infectious mononucleosis, acute CMV

infection, aseptic meningitis, and syphilis

D IAGNOSIS

■ ELISA/EIA and rapid HIV antibody tests: Detect antiviral antibodies;

used to diagnose HIV Usually  by three months after initial infection.

Because false-results may occur (especially in low-risk populations

be-ing screened), confirm by Western blot.

■ HIV RNA viral load: Not approved by the FDA for diagnosing HIV Has

high sensitivity even in patients who have not yet developed antibodies

False-results may occur, usually in the form of a low copy number (e.g.,

< 10,000 copies/mL); true-results in antibody-patients with acute

in-fection are usually > 100,000 copies/mL

■ p24 core antigen: Highly specific but less sensitive (85–90%) and less

readily available than HIV viral load Approved by the FDA for diagnosing

acute HIV

■ Detuned ELISA: Licensed for research only ELISA antibody- serum

samples are diluted and retested; if the ELISA test is after dilution, it

in-dicates a lower concentration, less specific antibodies, and seroconversion

within the last 4–6 months

T REATMENT

■ Current recommendations (International AIDS Society-USA, 2006) are

to start HIV treatment in all patients who are symptomatic Treatment

of asymptomatic patients should be started when the CD4 count is

200–350 cells/mm 3

■ Consider initiating antiretrovirals in patients with acute retroviral

syn-drome

■ Use three drugs—usually two nucleoside analogs (AZT, 3TC, d4T, ddI,

abacavir, tenofovir, emtricitabine) plus a non-nucleoside analog

(nevirap-ine or efavirenz) or a protease inhibitor (fosamprenavir, indinavir,

nelfi-navir, saquinelfi-navir, atazanelfi-navir, or lopinavir/ritonavir) that may be ritonavir

“boosted.” Protease inhibitors can have significant drug interactions

■ During pregnancy, women should be offered standard therapy in the

form of two nucleoside reverse transcriptase inhibitors (including AZT)

plus nevirapine or a protease inhibitor Consider starting after 10–14

weeks of gestation to minimize the risk of teratogenicity Efavirenz is

con-traindicated during pregnancy.

Do not use HIV viral load as a factor in deciding when to initiate antiretroviral therapy.

I N F E C T I O U S M O N O N U C L E O S I S

Caused by the Epstein-Barr virus (EBV) Commonly seen in late adolescenceand early adulthood (college or military populations) Clinical course is gen-erally benign, with patients recovering in 2–3 weeks

F I G U R E 1 1 3 Clinical decision points in HIV infection/disease in adults.

(Adapted, with permission, from Fauci AS et al Immunopathologic mechanisms of HIV

infec-tion Ann Intern Med 1996; 124:654.)

0 3 6 1 2 3 4 5 6 7 8 9 10 11

Clinical latency

Primary infection Constitutionalsymptoms

Opportunistic diseases Death

±Acute HIV syndrome Wide dissemination of virus Seeding of lymphoid organs

9 12

■ A maculopapular rash occurs in 10% of patients (especially in those given

ampicillin), and palatal petechiae may be seen RUQ tenderness is more

common than hepatomegaly

T A B L E 1 1 5 Prophylaxis Against AIDS-Related Opportunistic Infections

P ATHOGEN I NDICATIONS FOR P ROPHYLAXIS M EDICATION C OMMENTS

Pneumocystis CD4 count < 200/mm 3 or a TMP-SMX or dapsone +/− Single-strength tablets of

TMP-jiroveci history of oral thrush pyrimethamine or pentamidine SMX are effective and may be

pneumonia (PCP) Prophylaxis may be stopped if nebulizers or atovaquone less toxic than double-strength

on highly active antiretroviral therapy (HAART).

Mycobacterium CD4 count < 50/mm 3 Azithromycin, clarithromycin, Azithromycin can be given once

aviumcomplex Prophylaxis may be stopped rifabutin weekly Rifabutin can ↑ hepatic

months on HAART.

Toxoplasma CD4 count < 100/mm 3 and TMP-SMX or dapsone +/− Covered by all PCP regimens

ToxoplasmaIgG pyrimethamine or atovaquone except pentamidine.

Prophylaxis may be stopped

if CD4 > 100–200 for ≥ 3 months on HAART.

Mycobacterium PPD > 5 mm; history of a INH sensitive: INH × 9 months For INH-resistant strains, use

tuberculosis PPD that was inadequately (include pyridoxine) rifampin or rifabutin +/−

treated; close contact with a pyrazinamide.

person with active TB.

Candida Frequent or severe recurrences Fluconazole or itraconazole

HSV Frequent or severe recurrences Acyclovir, famciclovir, valacyclovir

Pneumococcus All patients Pneumococcal vaccine Some disease may be prevented

with TMP-SMX, clarithromycin, and azithromycin Repeat when CD4 >

200.

Influenza All patients Influenza vaccine

HBV All susceptible patients (i.e., Hepatitis B vaccine (three doses)

hepatitis B core antibody ) HAV All susceptible patients at ↑ Hepatitis A vaccine (two doses) IV drug users, men who have

risk for HAV infection or with sex with men, and hemophiliacs chronic liver disease (e.g., are at ↑ risk.

chronic HBV or HCV).

P RESENTATION D IAGNOSIS 1 ° T HERAPY T HERAPY O THER

Pneumocystis Nonproductive CXR frequently TMP-SMX Pentamidine or Maintenance

jiroveci cough, fever, and shows bilateral If P O2< 70 mmHg dapsone plus TMP therapy should be pneumonia dyspnea interstitial at room air, add or primaquine plus continued (PCP) Symptoms often infiltrates but prednisone clindamycin or following initial

progress over may be normal atovaquone therapy.

weeks CD4 is Hypoxia with often < 200 ambulation;

elevated LDH.

Confirm with organism seen

on silver-stained sputum sample

or bronchoscopy.

Mycobacterium Fever, night sweats, Pancytopenia, Clarithromycin Azithromycin plus Maintenance

aviumcomplex weight loss, elevated alkaline plus ethambutol ethambutol +/− therapy should (MAC) fatigue, diarrhea, phosphatase, low +/− rifabutin rifabutin be continued

adenopathy may reveal and hepato- diffuse lymph- splenomegaly adenopathy and may be seen hepato-

CD4 is often splenomegaly.

< 50 Diagnosed by

culture of the organism from a sterile site (blood

or lymph node).

Toxoplasma Fever, headache, Head CT with Pyrimethamine Pyrimethamine Leucovorin should

gondii altered mental contrast or MRI plus sulfadiazine plus clindamycin or be given with encephalitis status, seizure, with ring- TMP-SMX or pyrimethamine

and/or focal enhancing pyrimethamine Steroids should neurologic lesions (often plus atovaquone be given only if

< 100 be normal or

may show ↑ protein and mononuclear pleocytosis.

■ CMV: Consider if there was a recent blood transfusion Symptoms are

usually systemic; sore throat and lymphadenopathy are uncommon

Diag-nose with a CMV IgM

■ Heterophil- EBV: Usually affects children; has milder symptoms.

■ Acute toxoplasmosis: Presents with nontender head and neck

lym-T A B L E 1 1 6 Diagnosis and Treatment of Selected Opportunistic Infections in HIV/AIDS Patients (continued)

P RESENTATION D IAGNOSIS 1 ° T HERAPY T HERAPY O THER

Cryptococcus Meningitis: CSF: High opening Induction: Liposomal May require

neoformans Headache, pressure, Amphotericin B amphotericin B multiple LPs to

malaise, nausea, elevated protein, plus flucytosine plus flucytosine or relieve high ICP.

fever, visual low glucose, and × 14 days fluconazole plus Chronic changes, CN lymphocytosis Consolidation: flucytosine maintenance deficits, Twenty-five Fluconazole 400 therapy may be

be asymptomatic studies Fluconazole 200 treatment with

pulmonary CSF culture  indefinitely for six months

CD4 is often < 100 blood cultures

.

loss of vision, exam: Large foscarnet, or cause bone floaters plaques with cidofovir Consider marrow

Odynophagia exudates and ganciclovir may also cause

(watery or Endoscopy: severe retinitis myelitis, or

abdominal pain ulcerations; 10%

CD4 is often are normal

< 50 Confirm with

biopsy.

Crypto- Persistent watery Must request stool Initiation of HAART Possible benefit Symptomatic relief

sporidiosis diarrhea; exam for is the only from paromomycin with antimotility

occasional nausea, Cryptosporidia treatment shown to agents and vomiting, and/or (modified AFB, have benefit electrolyte fever Can cause trichrome, or DFA); repletion

CD4 < 100 standard O&P exam requires ERCP and

HAART.

and IgG seroconversion.

■ 1 ° HIV infection: Fever, lymphadenopathy, pharyngitis, maculopapular

rash, and, less commonly, aseptic meningitis

■ HAV or HBV: Characterized by markedly elevated AST and ALT.

■ Syphilis.

■ Rubella: A prominent rash begins on the face and progresses to the trunk

and extremities Has a shorter course (only several days)

■ Streptococcal pharyngitis: Presents with fever, tender submandibular or

anterior cervical lymphadenopathy, and pharyngotonsillar exudates with

no cough Splenomegaly is not seen Diagnose with rapid streptococcaltest and throat culture if antigen test is 

D IAGNOSIS

■ Neutropenia (mild left shift); atypical lymphocytes (see Figure 11.4) in

70% of cases (WBC 12,000–18,000 and occasionally 30,000–50,000);thrombocytopenia; mildly elevated LFTs

■ Heterophil antibodies (Monospot) are found in 90% of cases (may

ini-tially be  and then turn  in 2–3 weeks) Other EBV serologies arerarely needed

■ Anti-VCA IgM is at presentation; anti-EBNA and anti-S antibodies are

 in 3–4 weeks Anti-VCA IgG antibodies are  if patients were ously exposed Cold agglutinins are found in 80% of cases after 2–3 weeks

previ-T A B L E 1 1 7 Infection Control Measures

P RECAUTION T RANSMISSION OF B ARRIERS TO B E U SED (E XAMPLES )

Standard Transient flora from Hand washing; gloves for contact with all Everybody!

patients or surfaces body fluids and mucosa Face shields

and gowns if splashes of body fluids are possible.

Airborne Droplet nuclei (≤ 5 μm) Negative-pressure rooms and use of TB, measles, SARS, vesicular rashes

or dust particles that surgical masks when transporting (chickenpox, zoster, smallpox).

remain suspended for patients Health care workers should use long distances fitted N-95 masks Consider face shields.

Droplet Large droplets that Private rooms and use of surgical masks Meningococcal or H influenzae

travel < 3 feet and are when patients are transported Health meningitis, influenza, pertussis.

generated by coughing, care workers should use surgical masks.

sneezing, talking, suctioning, or bronchoscopy.

Contact Direct and indirect Private rooms (patients may be grouped Some fecally transmitted infections

contact together); limit patient transport (HAV, C difficile), vesicular rashes

Dedicated equipment (e.g., stethoscopes) (chickenpox, zoster, smallpox), SARS Health care workers should use gowns

and gloves for all patients.

No treatment is necessary in the majority of cases Steroids are used on rare

occasions for tonsillar obstruction, severe thrombocytopenia, autoimmune

he-molytic anemia, and CNS complications

C OMPLICATIONS

Autoimmune hemolytic anemia (< 3%) Splenic rupture is rare but may occur

in weeks 2–3 (patients should avoid contact sports and heavy lifting)

Menin-goencephalitis is rare, and patients usually recover completely

LY M E D I S E A S E

A tick-borne illness caused by Borrelia burgdorferi (found in the Northeast,

mid-Atlantic, and upper Midwest more than the West) and other Borrelia

species (found in Europe and Asia) Prevalence is based on the distributions

of the tick vectors Ixodes scapularis (found in the Northeast and upper

Mid-west) and I pacificus (found in the West) Transmitted primarily by nymphal

stages that are active in late spring and summer Requires tick attachment for

> 24 hours

S YMPTOMS /E XAM

■ Early localized infection: Occurs one week (3–30 days) after tick bite.

Presents with erythema migrans (60–80%), which appears as an

expand-ing red lesion with “bull’s eye” central clearexpand-ing on the thigh, groin, or

ax-illa (see Figure 11.5) Often accompanied by fever, myalgias, and

lym-phadenopathy

■ Early disseminated infection:

■ Occurs days to weeks after onset of the initial erythema migrans lesion

Skin lesions are like erythema migrans but are smaller and often multiple

■ Neurologic involvement may include cranial neuritis (CN VII palsy is

most common and may be bilateral), peripheral neuropathy, and/or

aseptic meningitis Cardiac abnormalities include AV block (rarely

re-quiring a permanent pacemaker), myopericarditis, and mild left

ven-tricular dysfunction

■ Migratory myalgias, arthralgias, fatigue, and malaise are common

dur-ing this phase

F I G U R E 1 1 4 Atypical lymphocytosis seen in infectious mononucleosis and other

infections.

These reactive T lymphocytes are large with eccentric nuclei and bluish-staining RNA in the

cytoplasm (Reproduced, with permission, from Braunwald E et al Harrison’s Principles of

In-ternal Medicine, 15th ed New York: McGraw-Hill, 2001.)

The rash of early Lyme disease, erythema migrans, is often missed and resolves in 3–4 weeks without treatment.

■ Late Lyme disease: Occurs months to years later in untreated patients.

Arthritis may develop in large joints (commonly the knee; shows PMN

predominance) or small joints Attacks last weeks to months with plete remission between recurrences and become less frequent over time.

com-Chronic neurologic findings include subacute encephalopathy (memory,sleep, or mood disturbances) and peripheral sensory polyneuropathy (pain

or paresthesias; abnormal EMG)

■ Congenital Lyme disease: Cases of congenital transmission resulting in

fetal death have been reported

D IAGNOSIS

The testing strategy depends on the pretest probability of disease (per theAmerican College of Physicians 1997 guidelines):

■ High likelihood ( > 80%, e.g., erythema migrans in an endemic area):

Clinical diagnosis is sufficient Serology is often  in early disease and isnot needed to confirm the diagnosis

■ Low likelihood ( < 20%, e.g., nonspecific complaints with no objective findings): Serologic testing is not indicated, and patients should not be

treated (results will likely be false s)

■ Intermediate likelihood (20–80%, e.g., some typical findings and dence in an endemic area): Combine ELISA with a confirmatory West-

resi-ern blot (as with HIV) In the first month of symptoms, test IgM and IgGantibodies in acute and convalescent sera; later, test only IgG antibodies

■ Patients with neuroborreliosis usually have a serum serology CSF body testing is not necessary

anti-■ PCR of plasma and tissue (but not CSF) is sensitive, but no guidelines ist

ex-T REATMENT

■ Early Lyme disease: Doxycycline or amoxicillin × 14–21 days (an tive is cefuroxime) In the presence of meningitis, radiculopathy, or third-

alterna-F I G U R E 1 1 5 Erythema chronicum migrans seen in Lyme disease.

The classic “bull’s eye” lesion consists of an outer ring where the spirochetes are found, an ner ring of clearing, and central erythema due to an allergic response at the site of the tick bite Note that some lesions may consist only of the outer annular erythema with central clearing.

in-(Reproduced, with permission, from Braunwald E et al Harrison’s Principles of Internal cine, 15th ed New York: McGraw-Hill, 2001.)

Medi-Lyme disease may present as

asymmetric oligoarticular

arthritis, frequently of the

knee or other large joints.

Ixodes scapularis bites can

lead to coinfection with Lyme

disease, human granulocytic

anaplasmosis, and/or

babesiosis.

degree AV block, treat with ceftriaxone or cefotaxime × 14–28 days (or,

al-ternatively, IV penicillin or doxycycline) Treatment response for early

Lyme disease is excellent Jarisch-Herxheimer reactions occur in 5–10% of

patients during the first days of treatment

■ Late infection (arthritis): Doxycycline or amoxicillin × 28 days For the

first arthritis recurrence, repeat doxycycline or ceftriaxone × 14 days For

further recurrences, treat symptomatically and consider synovectomy For

late neurologic disease, treat with ceftriaxone × 14–28 days; response may

be slow and incomplete

P REVENTION

Patients in endemic areas with a tick that is partially engorged or attached for

> 24 hours may benefit from doxycycline 200 mg PO × 1 dose Testing of

ticks for infectious organisms is not recommended Lyme disease vaccine is

no longer available

C OMPLICATIONS

■ Some patients may have treatment-resistant (autoimmune) arthritis for

months to years despite appropriate antibiotics B burgdorferi DNA is not

found in the joint, and patients do not respond to antibiotics

■ Following appropriately treated Lyme disease, some patients may develop

poorly defined, subjective complaints (myalgia, arthralgia, fatigue,

mem-ory impairment) These patients do not benefit from repeated or

pro-longed antibiotic treatment The most common reason for apparent

an-tibiotic failure in Lyme disease is misdiagnosis

M E N I N G I T I S

S YMPTOMS /E XAM

As for encephalitis Atypical presentations are more likely in neonates, young

children, and the elderly Etiologies are as follows:

■ Acute meningitis:

■ Acute neutrophilic meningitis: Caused by bacteria (see Table 11.8).

■ Acute eosinophilic meningitis: Caused by Angiostrongylus

cantonen-sis, or rat lung worm; results from ingestion of undercooked mollusks

or contaminated vegetables Endemic in Southeast Asia and the Pacific

Islands; associated with peripheral eosinophilia

■ Chronic meningitis:

■ Characterized by symptoms lasting from weeks to months with

persis-tent CSF pleocytosis (usually lymphocytic):

■ Etiologic agents include TB (40%), atypical mycobacteria,

Cryptococ-cus (7%), Coccidioides, Histoplasma, Blastomyces, 2° syphilis, Lyme

disease, and Whipple’s disease The etiology is frequently unknown

(34%) Noninfectious causes include CNS or metastatic neoplasms

(8%), leukemia, lymphoma, vasculitis, sarcoid, and subarachnoid or

subdural bleeds

■ Chronic neutrophilic meningitis: May be caused by Nocardia,

Actino-myces, Aspergillus, Candida, SLE, or CMV in advanced AIDS.

■ Chronic eosinophilic meningitis: Associated with Coccidioides,

para-sites, lymphoma, and chemical agents

■ Chronic meningitis and cranial nerve palsies: Caused by Lyme

dis-ease, syphilis, sarcoid (CN VII—Bell’s palsy), and TB (CN VI—lateral

rectus palsy)

Patients with a tick attached for < 24 hours do not need treatment for Lyme disease.

■ Also associated with HSV-2 (recurrent—Mollaret’s meningitis) as well

as with HIV and drug reactions (TMP-SMX, IVIG, NSAIDs, mazepine) Unlike HSV-1 encephalitis, HSV-2 meningitis has a benigncourse, but treatment and/or suppression can be considered

carba-■ Less common but treatable causes include 2° syphilis (penicillin),Lyme disease (ceftriaxone), and leptospirosis (doxycycline)

in-■ Subacute course and stable patients: Obtain a history and physical and

obtain a CT/MRI (if indicated), blood cultures, and LP; then give empirictreatment

■ Obtain a head CT/MRI before LP if a mass lesion is suspected (e.g., withpapilledema, coma, seizures, focal neurologic findings, or immunocom-promised patients)

■ CSF Gram stain sensitivity is 75% (60–90%); CSF culture sensitivity is

T A B L E 1 1 8 Initial Antimicrobial Therapy for Purulent Meningitis of Unknown Cause

C OMMON E MPIRIC A NTIBIOTICS —F IRST S EVERE P ENICILLIN

Adults 18–50 years of S pneumoniae, N meningitidis. Ceftriaxone/cefotaxime +/− Chloramphenicol + vancomycin c

Adults > 50 years of age S pneumoniae, Listeria Ceftriaxone/cefotaxime + Chloramphenicol (N.

monocytogenes,gram-bacilli ampicillin +/− vancomycin c meningitidis) + TMP-SMX

(Listeria)+ vancomycin c Impaired cellular S pneumoniae, Ceftazidime + ampicillin +/− TMP-SMX + vancomycin c

immunity (or alcohol L monocytogenes,gram- vancomycin c

abuse) bacilli (Pseudomonas).

Post-neurosurgery or S pneumoniae, S aureus, Ceftazidime + vancomycin Aztreonam or ciprofloxacin + post–head trauma gram-bacilli (including (for possible MRSA) vancomycin.

Pseudomonas ).

a May add steroids (dexamethasone 10 mg q 6 h × 2–4 days) for patients who present with acute community-acquired meningitis

that is likely to have been caused by S pneumoniae.

b Doses for meningitis are higher than those for other indications: ceftriaxone 2 g IV q 12 h, cefotaxime 2 g IV q 4 h, vancomycin

1 g IV q 12 h or 500–750 mg IV q 6 h, ampicillin 2 g IV q 4 h, or ceftazidime 2 g IV q 8 h.

c In areas where penicillin-resistant pneumococcus is prevalent, vancomycin should be included in the regimen.

Adapted, with permission, from Tierney LM et al Current Medical Diagnosis & Treatment, 44th ed New York: McGraw-Hill, 2005:

1251.

75% (70–85%) for bacterial meningitis (see Table 11.9) Sensitivity is

un-changed if antibiotics are administered < 4 hours before culture

P REVENTION

■ N meningitidis chemoprophylaxis: Given to household contacts,

room-mates, or cellmates; those with direct contact with the patient’s oral

secre-tions (kissing, sharing utensils, endotracheal intubation, suctioning, day

care contacts if < 7 days); and special cases (immunocompromised,

out-breaks)

■ Also given to index patients if not treated with cephalosporin (penicillins

and chloramphenicol do not reliably penetrate the nasal mucosa) Possible

regimens include rifampin 600 mg PO BID × 4 doses, ciprofloxacin 500

mg PO × 1 dose, or ceftriaxone 250 mg IM × 1 dose

■ N meningitidis vaccine (serotypes A, C, Y, and W-135, not B): Given

for epidemics as well as to military recruits, pilgrims to Mecca, and

travel-ers to the African Sahel (meningitis belt), Nepal, and northern India May

also be given to college freshman living in dormitories, asplenic patients,

and those with terminal complement (C5–C9) and properdin deficiencies

T A B L E 1 1 9 CSF Profiles in Various CNS Diseases

O PENING

D IAGNOSIS ( PER μL) ( PER μL) (mg/dL) (mg/dL) (cm H 2 O) A PPEARANCE

a Traumatic tap usually yields 1 WBC/800 RBCs and 1 mg protein/1000 RBCs.

b May have PMN predominance in early stages.

c May be seen with brain abscess, epidural abscess, vertebral osteomyelitis, sinusitis/mastoiditis, septic thrombus, and brain tumor.

■ H influenzae type b chemoprophylaxis: Give rifampin to household

con-tacts of unvaccinated children < 4 years of age; consider for day care concon-tacts

■ H influenzae type b vaccine: Routine childhood immunization; consider

in adult patients with asplenia

M I C R O B I O LO G Y P R I N C I P L E S

■ In clusters (sometimes chains or pairs): Staphylococcus.

■ Coagulase: S aureus.

■ Coagulase: Examples include S epidermidis and S saprophyticus.

■ In chains or pairs: Streptococcus.

■ Lancet-shaped pairs: S pneumoniae (see Figure 11.6).

■ In pairs: Enterococcus.

■ Large with spores: Bacillus, Clostridium.

■ Small, pleomorphic (diphtheroids): Corynebacterium, Propionibacterium.

■ Filamentous, branching, beaded:

This Gram-stained sputum sample shows many neutrophils and lancet-shaped gram- cocci

in pairs and chains, indicating infection with S pneumoniae (Reproduced, with permission, from Kasper DL et al Harrison’s Principles of Internal Medicine, 16th ed New York: McGraw-

Hill, 2005: 810.)

To remember

gram-positive cocci—

The Grapes of Staph

(like The Grapes of

Streptococci are often

seen in long strips or

chains.

■ Nonfermenters: Proteus, Serratia, Edwardsiella, Salmonella, Shigella,

Morganella, Yersinia, Acinetobacter, Stenotrophomonas, Pseudomonas.

■ Anaerobes: Bacteroides, Fusobacterium.

■ Fusiform (long, pointed): Fusobacterium, Capnocytophaga.

Nontuberculous (atypical) mycobacteria are natural inhabitants of water and

soil They can cause clinical disease in both immunocompetent and

immuno-compromised patients and are often difficult to diagnose and treat

S YMPTOMS /E XAM

■ Mycobacterium avium: Most frequently presents as cavitary upper lobe

lesions in patient with underlying pulmonary disease (COPD) However,

otherwise normal hosts can develop midlung nodular bronchiectasis In

HIV/AIDS patients, a systemic disease with fever, abdominal pain,

lym-phadenopathy, and hepatosplenomegaly is most frequently seen

■ Mycobacterium kansasii: Primarily a pulmonary pathogen presenting

in a manner similar to M tuberculosis Patients may or may not be

im-munocompromised and often have an underlying lung disease

■ Mycobacterium marinum: The 1° presentation consists of skin ulcers and

nodular lymphangitis in patients with exposure to freshwater and

saltwa-ter, including marine organisms, swimming pools, and fish tanks

■ Rapidly growing mycobacteria (M abscessus, M fortuitum, M

che-lonae): M abscessus is the most virulent of these pathogens, causing

nodular or cavitary pulmonary disease and often causing skin or soft

tis-sue infections Disseminated or localized skin and soft tistis-sue infections

are the most common clinical manifestation of M fortuitum (associated

with nail salons) and M chelonae.

D IFFERENTIAL

■ Cavitary or nodular lung disease: M tuberculosis, endemic mycoses

(coc-cidioidomycosis, histoplasmosis, blastomycosis, paracoccidioidomycosis),

Nocardia, aspergillosis, neoplasms.

■ Skin ulcers or nodular lymphangitis: Sporothrix schenckii, Nocardia

brasiliensis, M marinum, Leishmania braziliensis, Francisella tularensis

D IAGNOSIS

■ Pulmonary disease: All three of the following criteria must be satisfied.

■ Clinical criteria: Compatible signs and symptoms (cough, fatigue,

fever, weight loss) with reasonable exclusion of other diseases

■ Radiographic criteria: CXR with persistent or progressive infiltrates

with cavitation and/or nodules or CT with multiple small nodules or

multifocal bronchiectasis

To remember lactose-fermenting gram-negative rods—

biopsy with growth from a sterile site.

■ Nodular lymphangitis: Aculture from biopsy

T REATMENT

Treatment for these infections requires multiple drug regimens for prolongedcourses of therapy Many of these organisms (particularly the rapidly growingmycobacteria) are resistant to multiple antimicrobial agents Consultationwith a specialist is recommended

C OMPLICATIONS

Pulmonary disease can result in progressive lung cavitation and destructionwith dissemination Skin and soft tissue disease can be locally destructive orlead to disseminated infection

O ST E O M Y E L I T I S

Spread may be contiguous (80%) or hematogenous (20%)

■ Local spread: Occurs in diabetics and in patients with vascular

insuffi-ciency, prosthetic joints, decubitus ulcers, trauma, and recent surgery

neuro-■ Hematogenous spread: Affects IV drug users, those with sickle cell

dis-ease, and the elderly

Common causes are as follows:

■ Etiologic agents include S aureus and, to a lesser extent, coagulase-staphylococci (prosthetic joints or postoperative infections), streptococci,

anaerobes (bites, diabetic foot infections, decubitus ulcers), Pasteurella mal bites), Eikenella (human bites), and Pseudomonas (nail punctures

(ani-through sneakers)

■ Other causes: Salmonella (sickle cell), M tuberculosis (foreign

immi-grants, HIV), Bartonella (HIV), Brucella (unpasteurized dairy products).

■ By location: Pseudomonas affects the sternoclavicular joint and symphysis

pubis (in IV drug users); Brucella affects the sacroiliac joint, knee, and hip.

TB affects the lower thoracic vertebrae (Pott’s disease)

S YMPTOMS /E XAM

■ Contiguous spread: Local redness, warmth, and tenderness; patients are

afebrile and are not systemically ill

■ Hematogenous spread: Sudden fever; pain, and tenderness over the

af-fected bone May present with pain only (no fever)

■ Vertebral osteomyelitis with epidural abscess: Spinal pain followed by

radicular pain and weakness

■ Prosthetic hip and knee infections: May present only as pain on weight

usually includes at least three

sputum smear and culture

(preferably morning)

specimens.

■ Plain x-rays: Reveal bony erosions or periosteal elevation ≥ 2 weeks after

infection Less helpful in trauma or diabetic/vascular patients with

neu-ropathy (frequent stress fractures)

■ CT scans.

■ MRI: Approximately 90% sensitive and specific (abnormal marrow edema;

surrounding soft tissue infection) Especially useful for diagnosing

verte-bral osteomyelitis

■ Nuclear scans: Three- or four-phase studies with technetium-99 are

pre-ferred Most useful for distinguishing bone from soft tissue inflammation

when the diagnosis is ambiguous

■ Microbiology: Obtain bone culture at debridement or by needle

aspira-tion; sinus tract cultures are not reliable With hematogenous

osteo-myelitis,blood cultures may obviate the need for bone biopsy

T REATMENT

■ After debridement of necrotic bone (with cultures taken), empiric

antibi-otics should be chosen to cover the likely pathogens (see above)

■ IV antibiotics should be given for 4–6 weeks, although oral quinolones

may be equally effective in some circumstances

■ The choice of agent is guided by microbiology In patients who are not

candidates for definitive therapy, long-term suppressive antibiotics may be

used

■ Surgery is indicated for spinal cord decompression, bony stabilization,

re-moval of necrotic bone in chronic osteomyelitis, and reestablishment of

vascular supply

P REVENTION

Diabetics with neuropathy (detected by the 10-g monofilament test) should

be taught to examine their feet on a daily basis and should be examined by a

clinician at least once every three months

C OMPLICATIONS

Vertebral osteomyelitis with epidural abscess; chronic osteomyelitis

PY E LO N E P H R I T I S

Caused by the same bacteria as those responsible for uncomplicated UTI

With the exception of S aureus, most cases are caused by organisms

ascend-ing from the lower urinary tract; S aureus is most frequently hematogenous

and produces intrarenal or perinephric abscesses Renal struvite stones

(staghorn calculi) are frequently associated with recurrent UTI due to

urease-producing bacteria (Proteus, Pseudomonas, and enterococci).

S YMPTOMS

Presents with flank pain and fever Patients often have lower urinary tract

symptoms (dysuria, urgency, and frequency) that sometimes occur 1–2 days

before the upper tract symptoms They may also have nausea, vomiting, or

di-arrhea

E XAM

Exam reveals fever, CVA tenderness, and mild abdominal tenderness

or other GU surgery).

■ X-rays can detect stones, calcification, masses, and abnormal gas tions

collec-■ Ultrasound is rapid and safe

■ Contrast-enhanced CT is most sensitive but may affect renal function

C OMPLICATIONS

■ Perinephric abscess should be considered in patients who remain febrile2–3 days after appropriate antibiotics; UA may be normal and cultures .Patients are treated by percutaneous or surgical drainage plus antibiotics

■ Intrarenal abscesses (e.g., infection of a renal cyst) < 5 cm in size usuallyrespond to antibiotics alone

■ Diabetics may develop emphysematous pyelonephritis, which usually quires nephrectomy and is associated with a high mortality rate

re-R O C K Y M O U N TA I N S P OT T E D F E V E re-R

A tick-borne illness caused by Rickettsia rickettsii The vector is the tor tick, which needs to feed for only 6–10 hours before injecting the organ-

Dermacen-ism (a much shorter attachment time than for Lyme disease) Most

com-monly found in the mid-Atlantic and South Central states (not the Rocky

Mountain states) The highest rates are seen in late spring and summer and

in children and men with occupational tick exposures

pe-■ Patients may develop severe headache, irritability, and even delirium orcoma

D IFFERENTIAL

Meningococcemia, measles, typhoid fever, ehrlichiosis (HME or HGA), viralhemorrhagic fevers (e.g., dengue), leptospirosis, vasculitis

Fever and WBC casts on UA

are seen in pyelonephritis but

not in cystitis.

Think of Rocky Mountain

spotted fever and start

treatment early in patients

with a recent tick bite

(especially in the mid-Atlantic

or South Central states) along

with fever, headache, and

myalgias followed by a

centripetal rash.

■ Diagnosis is made clinically (symptoms and signs plus recent tick bite);

treatment should be started as soon as Rocky Mountain spotted fever is

suspected

■ Diagnosis can be made by biopsy of early skin lesions or confirmed

retro-spectively by serologic testing

■ Labs may show thrombocytopenia, elevated LFTs, and hyponatremia The

Weil-Felix test (for antibodies cross-reacting to Proteus) is no longer

Table 11.10 outlines STDs that result in genital ulcers as well as urethral or

cervical discharge Refer to the Women’s Health chapter for further discussion

of STDs, cervical cancer screening, and chlamydia screening

ST R O N G Y LO I D I A S I S

Infection with the helminth Strongyloides stercoralis is endemic in warm

cli-mates such as the southeastern United States, Appalachia, Africa, Asia, the

Caribbean, and Central America Unlike most other parasitic worms,

Strongy-loides can reproduce in the small intestine, leading to a high worm burden.

Autoinfection and dissemination are seen in hosts with deficient cell-mediated

immunity (e.g., AIDS, chronic steroids, organ transplants, leukemia,

lym-phoma)

S YMPTOMS /E XAM

■ Normal hosts: May be asymptomatic or present with vague epigastric

pain, nausea, bloating, diarrhea, or weight loss due to malabsorption

Ser-piginous papules or urticaria (“larva currens”) may be seen around the

buttocks, thighs, and lower abdomen as larvae migrate from the rectum

and externally autoinfect the host

■ Immunocompromised hosts: Hyperinfection or disseminated

strongyloidi-asis can develop Worms leave the GI tract and travel to the lungs and

else-where Patients present with fever, severe abdominal pain, dyspnea,

produc-tive cough, hemoptysis, and local symptoms (e.g., CNS, pancreas, eyes)

D IFFERENTIAL

Local enteric disease mimics PUD, sprue, or ulcerative colitis Hyperinfection

resembles overwhelming bacterial or fungal sepsis

D IAGNOSIS

■ Stool or duodenal aspirates can be tested for ova and parasites In

hyperin-fection, larvae may be seen in sputum, bronchoalveolar lavage, CSF, and

urine Paradoxically, eosinophilia is prominent in normal hosts with

dis-Consider hyperinfection with Strongyloides stercoralis in patients with vague abdominal complaints or fleeting pulmonary infiltrates plus eosinophilia, or in immunosuppressed patients who develop systemic gram-

or enterococcal infection.

T A B L E 1 1 1 0 Diagnosis and Treatment of Selected STDs

D ISEASE P ATHOGEN C LINICAL P RESENTATION D IAGNOSIS T REATMENT O PTIONS Causes of genital ulcers:

Chancroid Haemophilus ducreyi Painful erythematous Gram stain shows small Drain buboes

papule evolving into a gram-rods in parallel Azithromycin 1 g PO

pustule that erodes into alignment (“school of × 1, ceftriaxone 250 mg

an ulcer with purulence fish”); culture, PCR IM × 1, ciprofloxacin

500 mg PO TID ×

7 days.

HSV Human herpes Painful multiple Tzanck smear shows Acyclovir 400 mg PO

simplex virus 1 or 2 vesicular or ulcerative multinucleated giant cells TID or 200 mg PO

lesions Reactive (50% sensitivity); culture, 5ID × 7–10 days,

lymphadenopathy is DFA, PCR, IgG ELISA famciclovir 250 mg PO

valacyclovir 1 g PO BID

× 7–10 days.

Consider suppressive or episodic treatment for recurrent infection.

Granuloma Klebsiella Painless, progressive Culture is low yield Doxycycline 100 mg PO

inguinale granulomatis ulcerative lesions Biopsy shows dark- BID × ≥ 3 weeks and

(formerly known as without regional staining Donovan bodies until all lesions have

Calymmatobacterium lymphadenopathy PCR is available. completely healed.

granulomatis) Beefy-red ulcers bleed Alternative regimens

on contact Rare in the include azithromycin, United States; endemic in ciprofloxacin,

TMP-SMX for ≥ 3 weeks until all lesions have completely healed.

Lympho- Chlamydia Painless, small ulcer at Culture is low yield; Drain buboes

granuloma trachomatis(serovars the site of inoculation serology is most Doxycycline 100 mg PO

venereum L1, L2, or L3) Large, tender, fluctuant, commonly used PCR is BID or erythromycin

disease may result in hemorrhagic proctocolitis

Strictures and fistulae may form.

T A B L E 1 1 1 0 Diagnosis and Treatment of Selected STDs (continued)

D ISEASE P ATHOGEN C LINICAL P RESENTATION D IAGNOSIS T REATMENT O PTIONS

Syphilis Treponema pallidum Painless solitary ulcer Darkfield microscopy, For 1 ° syphilis:

(rarely multiple) May DFA of tissue RPR/VDRL Benzathine penicillin

have painless, rubbery confirmed by FTA-ABS G 2.4 million

lymphadenopathy (RPR/VDRL may take 12 U IM × 1.

weeks to turn ) For penicillin-allergic

patients, give doxycycline 100 mg

PO BID × 14 days or tetracycline 500 mg

PO QID × 14 days.

Causes of urethritis and cervicitis:

Gonococcal (GC) Neisseria Purulent discharge May Gram stain of urethral or Ceftriaxone 125 mg IM

gonorrhoeae have pharyngitis, cervical swab shows × 1, cefpodoxime 400

Disseminated GC diplococci (see Figure 500 mg PO × 1, ofloxacin infection is associated 11.7) 400 mg PO × 1, or with two syndromes: Culture on Thayer-Martin levofloxacin 250 mg PO (1) fever, tenosynovitis, media, nucleic acid × 1 plus treatment for

and painful amplification test chlamydia if chlamydial

vesiculopustular skin (NAAT), DNA probe. infection is not ruled

lesions or (2) purulent out.a arthritis without skin

lesions.

Nongonococcal Chlamydia Mucoid or watery Urethritis: Mucopurulent Azithromycin 1 g PO

common pathogens Other syndromes include Gram stain of urethral PO BID × 7 days

include Mycoplasma proctitis, epididymitis, secretions shows > 5 Alternative regimens

genitalium,HSV, and PID Has a known WBCs/hpf plus include erythromycin,

Trichomonas association with leukocyte esterase on ofloxacin, or levofloxacin

vaginalis,and postinfectious reactive first-void urine × 7 days.

Ureaplasma arthritis. Chlamydia trachomatis:

urealyticum. NAAT on the urethra,

vagina, or urine; culture.

a Quinolones are no longer recommended by the CDC for treatment of GC infections in the United States due to high rates of

resis-tance.

■ 1 ° syphilis: Usually presents with a chancre, a single painless papule that

erodes to form a clean-based ulcer with raised/indurated edges (may bemultiple or atypical for HIV-patients or minimal for those with previous

syphilis) Also presents with regional nontender lymphadenopathy The

incubation period is three weeks (ranging from three days to threemonths) The chancre resolves in 3–6 weeks, but lymphadenopathy per-sists

■ 2 ° syphilis:

■ Presents with a maculopapular rash that may include the palms and soles; condylomata lata in intertriginous areas (painless, broad, gray-

ish-white to erythematous plaques that are highly infectious; see Figure

11.9); alopecia (see Figure 11.10); or a mucous patch (condylomata

lata on the mucosa)

F I G U R E 1 1 7 Gonococcal urethritis: Gram stain of Neisseria gonorrhoeae.

Multiple gram-diplococci are seen within PMNs as well as in the extracellular areas of a

smear from a urethral discharge (Reproduced, with permission, from Wolff K et al Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed New York: McGraw-Hill, 2005: 906.)